Metabolic Improvement of Poorly Controlled Noninsulin-Dependent Diabetes Mellitus Decreases Bone Turnover1
Author(s) -
Ryo Okazaki,
Yasuo Totsuka,
Kumiko Hamano,
Miho Ajima,
Masakazu Miura,
Yoshiko Hirota,
Keishi Hata,
Seiji Fukumoto,
Toshio Matsumoto
Publication year - 1997
Publication title -
the journal of clinical endocrinology and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.206
H-Index - 353
eISSN - 1945-7197
pISSN - 0021-972X
DOI - 10.1210/jcem.82.9.4258
Subject(s) - medicine , endocrinology , bone remodeling , deoxypyridinoline , osteocalcin , bone resorption , n terminal telopeptide , glycemic , diabetes mellitus , parathyroid hormone , metabolic control analysis , chemistry , alkaline phosphatase , calcium , biochemistry , enzyme
Patients with poorly controlled noninsulin dependent diabetes mellitus (NIDDM) are shown to have higher bone mass. However, the influence of changes in glycemic control on bone turnover is not known. To clarify whether metabolic improvement of poorly controlled NIDDM affects bone turnover, markers for glucose, mineral, and bone metabolism were assessed before and after glycemic control for 3 weeks in 78 poorly controlled NIDDM patients with initial hemoglobin A1c over 8%. Metabolic improvement caused a reduction in urinary calcium (Ca) and phosphate (Pi) and serum 1,25(OH)2D levels, and an increase in serum Pi without changes in serum Ca or parathyroid hormone levels. Bone resorption markers, urinary deoxypyridinoline (Dpd) and type I collagen carboxy-terminal telopeptide (CTx), as well as a bone formation marker, serum bone type alkaline phosphatase (BALP), were reduced. However, another bone formation marker, serum osteocalcin (OC), was low before treatment and was elevated after treatment. The decrease in Dpd, CTx and BALP, but not the increase in OC, correlated with each other and with the improvement in glycemic indices. In conclusion, metabolic improvement of poorly controlled NIDDM decreases bone turnover within a short period. Thus, glycemic control may protect NIDDM patients from bone loss. It is possible that serum OC is affected by hyperglycemia per se, and may not correctly reflect bone turnover.
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